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Dr. Barr MSP Final
Dr. Barr's NYCC MSP Final Exam
| Question | Answer |
|---|---|
| What are the 4 spondyloarthropathies? | 1. Ankylosing spondylitis 2. Psoriatic arthritis 3. Reiter's syndrome 4. Enteropathic arthropathy |
| What are the general characteristics of spondyloarthropathies? | Seronegative Affect the spine (not just c-spine) Asymmetric involvement Few peripheral joints involved Inflam of tendons and fascia Younger males HLA-B27 |
| What are other names for ankylosing spondylitis? | Rheumatoid spondylitis and marie-struempell Dz |
| Where does ankylosing spondylitis usually appear? | Mainly localized to the spine; peripheral joint involvement in 1/3 patients; starts in SI joints and pt. dependent on severity |
| Who gets ankylosing spondylitis? | 1:200 people; 8:1 males:females; age of onset is 15-30 y/o; 20% chance sibling has AS. |
| Describe the pathogenesis of ankylosing spondylitis. | Inflam of jts: syn. jts dev. pannus and cartilage jts dev. granulation tissue; spinal ligaments involved; chronic inflam of ligaments can -> granulation tissue deposit; pannus -> fibrous ankylosis -> bony; calcification of ligaments & granulation tissue |
| What are common areas of involvement of ankylosing spondylitis? | SI joint (starts) Spine Heels (calc @ achilles insert) Hips Shoulders |
| What do patients w/ AS complain of? | Initially: transient Sx and may only c/o stiffness; pain and stiffness over SIs (bilat.)Decreased chest expansion; pain at night, often severe and relieved by movement. |
| What is enthesopathy? | Local ligament or tendon fiber disruption; reactive bone forms at the end of ligament or tendon (enthesophyte) contributes to bony ankylosis. |
| How do advanced AS patients present? | Kyphotic posture; radiographic presentation of bamboo sign or dagger sign or trolley track sign. |
| What would laboratory findings be in a pt. w/ AS? | ESR: elevated (until ankylosis occurs) Alk Phos: normal RF: seronegative HLA-B27: positive |
| What causes bamboo sign? | Outer annular fibers ossify |
| What causes dagger sign? | Granulomatous change connects SPs (central) |
| What makes up trolley track sign? | Combo of dagger sign w/ fusion of Z-joints. |
| What is found in all spondyloarthropathies? | Sacroiliitis |
| When does AS in children appear, what is affected and how differentiate from JRA? | late childhood (8-10); SI findings on film same as older population; spares hands, wrists and c-spine; RF negative and HLA B27 positive. |
| Who gets psoriatic arthritis and when does the psoriasis and arthritis appear? | 10% of patients w/ psoriasis; psoriasis usually dev. b/w ages 10 & 30; Arthritis appears b/w ages 20 & 40 |
| Describe psoriasis including what it is and where it's located. | Abnormal proliferation of keratinocytes, doubling time greatly reduced; usually located on elbows, knees and scalp. |
| Describe the pathogenesis of psoriatic arthritis. | Pannus dev->fibrous ankylosis->bony ankylosis |
| How does someone w/ psoriatic arthritis present? | Psoriasis; SI or extremity joint pain, swelling or stiffness; finger or toenail changes (pitting); flares int eh skin will increase joint symptomspain similar to RA and AS; more extremity involvement; sausage digits. |
| What would lab results be in someone w/ psoriatic arthritis? | ESR: elevated Alk Phas: normal RF: seronegative HLA B27: elevated |
| What are radiographic findings in someone w/ psoratic arthritis? | Soft tissue swelling Normal bone density Uniform narrowing of jt space "fluffy" periostitis "Mouse ears" or "pencil in cup" deformity Spinal ankylosis in 20-40%; syndesmophytes asymmetrical & thinner - paravertebral ossifications |
| How might someone w/ juvenile psoriatic arthritis present? | Age b/w 9 & 12; 3:2 females:males; skin and nail changes; sausage digits; hip involvement. |
| What is the triad in Reiter's syndrome and who gets it most often? | Arthritis Conjunctivitis Urethritis (can't see, can't pee, can't dance w/ me); MC in young males |
| When does Reiter's syndrome usually appear? | 1-4 weeks after veneral exposure or dysentery. |
| What is the earliest Reiter's syndrome and what follows? | Urethritis (burning and frequency); Perfuse watery diarhea can precede urethritis; conjunctivitis is mild and bilat and can last days - weeks. |
| What can appear w/ Reiter's syndrome and where is the arthritis? | Painless rash on palms, soles and oral mucosa; asymmetrical, involves knees, ankles, achilles tendonitis and SI joints |
| What would lab results be for someone w/ Reiter's syndrome? | ESR: elevated HLA B27: elevated RF: seronegative |
| Reiter's radiographic findings are identical to which pathology? | Psoriatic arthropathy |
| What is enteropathic arthritis associated w/? | Ulcerative colitis and Crohn's Dz |
| How does enteropathic arthritis begin? | Monoarthritis (asymmetrical); mainly migratory and transient peripheral arthritis that subsides in 6 weeks. |
| What usually precedes arthritic symptoms in enteropathic arthritis and what is the "cause"? | Diarrhea; microorganisms, leaky gut, autoimmune |
| What is known to aggravate enteropathic arthritis, when are gut symptoms increased and what is Tx? | Milk and gluten; before and during arthritis attacks; antibiotics, bowel resection in ulcerative colitis, symptomatic management. |
| Enteropathic Arthritis is radiographically identical to what pathology? | Ankylosing spondylitis (particularly bamboo sign) |
| What is included in Crystal deposition joint diseases? | Gouty arthritis Pseudogout |
| What is gout characterized by? | Group of diseases characterized by crystalline deposition throughout the body; crystals composed of uric acid and high levels of uric acid present in blood |
| What is the problem in gout? | overproduction or inability to dispose of metabolic byproducts |
| Who gets gout more often and why? | Males:females 9:1; males have higher level of uric acid |
| What does gout typically demonstrate? | Hyperuricemia, recurrent attacks of acute arthritis (severe pain), remission of varying lengths, development of chronic tophi (accum. of uric acid crystals in the skin) |
| How does a pt. present w/ gout? | 90% have acute arthritis; podagra but can involve instep, heel, ankle, knee and wrist; cardinal signs of inflam.; pain begins at night and builds rapidly |
| 10-15% of gout pt. have chronic gout, what does this involve? | Pannus production and destruction; renal impairment; tophi dev. in soft tissue |
| What can exacerbate gout? | Stress: physical, emotional, alcohol abuse |
| What are treatments for gout? | NSAIDs Colchicine Corticosteroids Allopurinol |
| What is CPPD and what my it simulate? | Calcium pyrophosphate dihydrate crystal deposition (pseudogout); gout, RA, DJD, NA |
| When is the onset CPPD and how is it similar to DJD? | After 30 y/o and peaks at 60 y/o; chronic progressive joint pain, reduced ROM and crepitus. |
| Where is crystal deposition in CPPD? | Predominantly in peripheral joints: knees, wrists, hands; deposit in cartilage, synovium, tendons and ligaments. |
| What is evident on film for CPPD? | Calcium deposition in cartilage and haziness in joint space. |
| What are the systemic conditions that affect joints? | Lyme Dz Systemic Lupus Erythematosus |
| What can lyme Dz present like? | the "great mimicker": lupus, HIV, flue, RA, MS, EBV, Reiter's syndrome, meningitis, clinical depression, any infection. |
| What are early symptoms of Lyme Dz? | Rashes (bulls-eye typically) Fatigue HA Neck stiffness Jaw discomfort Pain/stiffness in mm of joints Slight fever Swollen glands Conjunctivitis |
| What are later symptoms of Lyme Dz? | Heart, nervous system or joint complications; MC late symptom is joint pain and swelling that is migratory and transient; movement painful but minimal cartilage and bone damage. |
| When could heart symptoms appear w/ Lyme Dz and what can they include? | 1-3 weeks after rash; dizziness, weakness, irregular heart beat |
| When could nervous system problems appear w/ Lyme Dz and what can they include? | 1 month after Dz onset; intermittent HA, difficulty concentrating/sleeping, irritability, neck stiffness, poor motor coordination; later: parasthesias in extremities, more difficulty concentrating, weakness in UE or LE, depression. |
| What is SLE, what does it affect and who gets it more often? | Multisystem autoimmune Dz; 9:1 F:M; more prevalent in black females; onset late teens to 40 y/o. |
| What is the etiology of SLE? | Probably genetic, may be induced by some medications (pain killers and antibiotics), may be triggered by exposure to UV light |
| What occurs w/ SLE to vasculature? | Deposition of immune complexes and fibrinoid materials in small arteries and arterioles, acute necrotizing vasculitis, thickening and narrowing of blood vessels. |
| What are SLE effects on the skin? | Erythema Butterfly rash over bridge of nose and cheeks Sunlight accentuates lesions May show on neck, elbows and dorsum of hands. |
| What are SLE effects on the kidney? | Glomerular damage Renal failure |
| What are other effects of SLE? | Alopecia (hair loss) Acute vasculitis of serosal membranes that may -> ulceration JOint involvemnt in 90% of patients (non-erosive synovitis) |
| How does SLE often present? | Self limiting rheumatic disorder; fever, malaise, anorexia, weight loss, polyarthralgia and skin rash; rarely spontaneous tendon rupture; bilat and symmetrical joint involvement; pain and swelling like RA, reversible sublux. in hands and C1-2 instabilit |
| Different parts of muscle are surrounded by a mysium, what is surrounded by what? | Muscle surrounded by epimysium Fasciculus surrounded by perimysium Muscle fiber surrounded by endomysium |
| What is the cell structure of skeletal muscle? | Long, multinucleated; sarcolemma is a thin, elastic, noncellular membrane that envelopes the cell; presence of myofilaments give a striated appearance to m. and are arranged in a basic contractile unit: sarcomere |
| What is contained in a sarcomere? | Half of 2 I bands, a central A band, the H zone that has the M line running through the center of this zone. |
| How are filaments arranged in a sarcomere? | thin filaments form a hexagonal array around each thick filament; each thin filament is equidistant from 3 thick filaments. |
| What is sarcoplasm? | A fluid that contains myoglobin, glycogen and fat droplets, phosphate compaounds and other small molecules/ions; myofilaments embedded w/in. |
| What is the sarcoplasmic reticulum? | A fraction of the sarcoplasm, it regulates Ca ion flow, surrounds each myofibril and terminal cisternae of SR closely approximate the T-tubules to form a triad. |
| Describe the movement of Ca ions guided by the SR. | With depolarization the SR passively releases Ca ions into the cell; w/ cessation of neural activity, the SR actively transports Ca back into the cisternae. |
| What is contained in the thin filament? | Actin: a glomerular protein Tropomyosin: a rod-shaped protein |
| Describe an actin monomer | Bead-like, associate into 2 strands that twist together in a helix. |
| Describe a tropomyosin monomer. | Composed of 2 rod shaped molecules twisted tog. to form a helix; each molecule is associated w/ 6 or 7 actin monomers in the actin filament; tropomyosin molecules lay end to end along the groove in the actin helix |
| What is the most important regulatory protein in striated muscle? | Troponin (TnC) |
| What is troponin? | Small globular protein; linked to tropomyosin at one of the molecule's ends. |
| What makes up the troponin complex? (3) | 3 globular subunits: TnT: attaches troponin to tropomyosin TnC: binds Ca ions TnI: inhibits actin-myosin interaction |
| What is the thick filament? | Called myosin, made up of 6 different polypeptides and a tertiary globular protein that makes up the head of the myosin filament. |
| How are the 6 polypeptides composing the myosin filament seperated? (3 sets) | 1 set of heavy chain proteins and 2 sets of light chain proteins that are associated w/ the globular head |
| How is myosin arranged? | Aggregate in the sarcoplasm to form thick filaments; they associate in pairs, end to end; these pairs grouped together in triplets; many triplet sets aggregate to form the myosin filament; each myosin head set are rotated 60 degrees from preceding set. |
| How do myosin heads look in a cross section? | Hexagonal presentation |
| What is the sliding filament theory? | Changes in muscle length occur by relative sliding movements b/w actin and myosin filaments; while muscle shortens, length of filaments remains constant. |
| What are the "steps" of the crossbridge cycle in the sliding filament theory? | Rest, Excitation, Contraction, Relaxation (APs control how many cycles occur) |
| Describe the rest step of the sliding filament theory. | No interaction b/w actin and myosin; troponin-tropomyosin complex block the binding site on actin; muscle resistance to passive extensibility is modest. |
| Describe the excitation step of the sliding filament theory. | Motor nerve stimulates the muscle and propagation of the AP depolarizes the cell through the T-tubule system; Event makes the membrane of the SR permeable to Ca and Ca floods into the sarcoplasm |
| What is excitation-contraction coupling? | The process by which depolarization of the muscle fiber initiates contraction; this step takes an electrical signal and converts it to mechanical action |
| Describe the excitation-contraction coupling step of the sliding filament theory. | AP is transmitted to all fibrils in the cell via the T-tubule system; triggers the passive release of Ca from the SR; Ca floods into the sarcoplasm and binds w/ TnC |
| What are the receptors present in excitation-contraction coupling? | Dihydropyridine receptor: voltage sensor; Ryanodine receptor: Ca release |
| What begins the contraction step in the sliding filament theory? | Binding of Ca to TnC causes a change in the troponin-tropomyosin-actin complex; blockade of the actin binding site is removed as the tropomyosin rod moves down into the groove b/w actin. |
| What is the middle part of the contraction step in the sliding filament theory? | Myosin heads move out perpendicularly from the filament towards the actin and bind; Myosin heads undergo an energy yielding conformational change; Actin filaments are pulled along the myosin filaments. |
| What completes the contraction step of the sliding filament theory? | The myosin head disassociates from the actin filament; If depolarization is maintained, crossbridge cycle will begin again and contraction continues; if depolarization stops then relaxation begins. |
| Describe the relaxation step in the sliding filament theory. | In the absence of an electrical signal, Ca is actively transported back into the SR; Blocking function of troponin-tropomyosin reestablishes itself, covering the actin binding site and inhibiting crossbridge interaction |
| What happens in the rest step of the sliding filament theory? | ATP has been bound to the myosin head. Myosin ATPase acts on the ATP and converts it to ADP-Pi form. No hydrolysis, no energy release...the head is "primed" and wants to bind to actin. |
| How is an actomyosin complex formed? | With depolarization, Ca is released into the cell and binds w/ TnC. The barrier to the actin binding site is removed and the "primed" myosin head binds to actin. At this instant in time an actomyosin complex is formed. |
| What occurs w/ excitation to get ADP and Pi released from myosin into the sarcoplasm? | Actomyosin ATPase completes the hydrolysis, breaking ADP and Pi apart. This hydrolysis liberates energy (releases Phosphate), and a conformational change in the myosin head occurs, pulling actin across myosin. |
| What occurs to get the myosin head to disassociate from actin? | As ADP and Pi are liberated it opens the ATP binding site on the myosin head. ATP binds to myosin, and in this form causes the myosin head to disassociate from actin. |
| What happens if there is no ATP available and what condition would give this situation? | No separation; rigor mortis: break down frees Ca and slowly muscles stiffen and further degeneration causes final flaccidity. |
| What causes the myosin and actin to bind again in excitation of sliding filament theory? | with the filaments separated myosin ATPase acts on the ATP and converts it to the ADP-Pi form. In this form myosin has a strong affinity to bind to actin. |
| How long will excitation go on? | As long as the depolarizing even continues; if depolarization stops, relaxation begins. |
| How does relaxation begin? | For relaxation to occur, Ca must be pumped back into the SR. As Ca is moved out of the sarcoplasm, the troponin-tropomyosin complex will block the actin binding site. |
| What makes up the membrane of the SR and how much Ca is sequestered? | The membrane consists almost entirely of pumps that have high affinity for Ca. Through active transport, 2 mol Ca are sequestered for each mol of ATP hydrolyzed. |
| What protein is inside the SR and how many Ca ions can it bind? | Calsequestrin; 43 Ca ions w/ moderate affinity. |
| Why is Calsequestrin good to the process of pumping Ca back into the SR? | Lowers Ca concentration using less ATP to keep Ca around. |
| What is the link b/w excitation and contraction of skeletal muscle? | Calcium |
| Will changes in extracellular Ca affect SR Ca levels? | No! The Ca is "on board" the skeletal muscle. |
| What do extracellular Ca changes affect? | Nervous system that affects muscle activity. |
| What does a crossbridge do? | During its action it exerts a longitudinal force for a certain distance, moving the actin fiber down the myosin fiber. |
| What is active stress (tension) proportional to? | The overlap b/w thick and thin filaments. Stress (tension) is proportional to the number of active crossbridges that can interact w/ the thin filament. |
| What happens as the muscle is stretched beyond its optimal length where maximum force can develop? | The stress decreases linearly w/ the overlap b/w actin and myosin. |
| What happens at the peak of the length-tension curve? | A small segment where tension does not change w/ length. |
| What lowers tension at sarcomere lengths that are less than optimal? | Force declines at sarcomere lengths that are less than optimal. Control mechanisms for the contractile machinery become less sensitive to stimulus at short muscle lengths, contributing to lower tension. |
| How must crossbridges attach and detach if a sarcomere shortens and what do the cycling rates depend on? | Asynchronously; primarily on the load (one end very little resistance and other has high resistance) |
| What are the factors that shortening velocities depend on? | 1. Velocity varies w/ the number of sarcomeres in a cell 2. Velocity depends on the load on the muscle. Crossbridge cycling rates fall as the stress on crossbridge increases; the conformational change in the myosin head is opposed by the load. |
| Why are there physiological differences in speed of contraction? | Molecular properties of myosin |
| What are the molecular properties of myosin that differ in the speed of contraction? (4) | 1. ATPase activity in m. 2. Construct of light chain proteins assoc. w/ myosin head 3. Amount of Ca released 4. Membrane potential |
| What is the mechanical threshold for Ca release? | When the membrane potential becomes less negative than -50 mV. |
| When does maximal Ca release occur? | Maximal Ca release occurs at -20 mV. |
| What makes the action potential/activation longer and what drug exhibits both longer AP and contractile response? | Agents that lower the mechanical threshold or prolong the AP increase the magnitude of the Ca pulse; Release of a greater amt of Ca potentiates the contractile response to a single AP; Caffeine does both |
| What is a twitch and why does this occur? | Submaximal response to a single AP; Enough Ca released to activate contractile machinery; Ca rapidly pumped back into the SR before the muscle has time to dev. max. force then twitch occurs (submaximal) |
| What produces a partial or complete tetanus? | Time relationships b/w the AP, Ca pulse and force dev. in skeletal m., repetitive AP cause a summation of twitches -> partial or complete tetanus. |
| What must occur before the maximal force is registered at the tendons? | Since force development is much slower than Ca release and binding to troponin b/c a number of crossbridge cycles must occur before the max force is registered. |
| What does the makeup of muscle (proteins) allow it to do? | Structural element is elastic and lengthen when a force is generated. |
| What is the Series Elastic Component? | Before force can be exerted on a load, this must be stretched. With a muscle twitch, much of the tension produced is used to stretch this component. |
| What occurs w/ repetitive stimuli during muscle contraction? | A greater proportion of the tension produced by the crossbridges may be measured as external force. Once the elastic component is stretched, all contractile tension may be exerted on the load (summation thru tetanus or activity) |
| How can intact muscle be stimulated? | Electrically (EMG) Chemically (motor n.) Mechanically (bruise eliciting contraction) |
| What is a myogram and what does it consist of? | A record of muscular events when looking at m. function; Latency period, contraction phase and a relaxation phase, changes in length of these phases depends on the muscle being evaluated and type of contraction being elicited. |
| What are the 4 types of contraction? | 1. Shortening 2. Lengthening 3. Isometric 4. Isokinetic |
| Describe a shortening contraction. | AKA dynamic or concentric contraction; Origin is moving toward insertion and the m. shortens in length, m. moves through acceleration, constant velocity and breaking phases w/ tension varying in each phase. |
| Describe a lengthening contraction. | AKA eccentric contraction; While the m. is contracting, the origin and insertion move farther apart |
| Describe a isometric contraction. | Implies same length; Tension is developed in a contracting m. but no visible shortening of muscle occurs. Origin and insertion are "fixed". |
| Describe a isokinetic contraction. | A true isotonic contraction (same tone or tension) in which a m. shortens at a constant velocity; only occurs when instrumentation is employed to control these variables over entire ROM. |
| How are muscles composed? | Functionally, not composed of homogenous tissue, most built of fibers w/ different mechanical and contractile properties; m. fivers divided into 2 main classes based on time it takes to reach peak tension |
| What are the current terms and old terminology for muscle fiber types? | Current: Type I and Type II fibers Old terminology: Slow twitch/Red fibers and Fast twitch/white fibers |
| What do type I, IIa and IIb fibers burn for energy? | I: fat burning IIa: both fat and glycogen burning IIb: glycogen burning |
| How are muscle fibers classified? | Based on histochemistry and histology including myosin composition, troponin structure, amount of SR, mitochondria and metabolic characteristics. |
| What determines the proportion of type I vs type II fibers? | Genetics; fiber differentiation begins week 20 in utero and nearly complete by 1 y/o; NS influences the fundamental dynamic properties of the muscle fiber. |
| What size are the motor neurons for type I and II fibers? | Type I motor neurons are smaller in diameter w/ slower conduction rates relative to those that innervate type II fibers (thicker and faster). |
| What does cross innervation do to muscles in studies? | type I will transform to type II and vice versa; nerves changed muscle type |
| What did a study involving electrodes on motor nerves show? | With electrical frequency changed the same result of fiber changes occurred. Neural signals determines skeletal muscle cell result. |
| Why was it more difficult to transform type I fibers to type II? | Intermediate type IIs have capability to behave like Is for ease of changing took longer going the other way but it still developed the characteristics of type II. |
| Why does "nervous system dictates" the muscle fibers make sense? | The pattern of nervous activity is important for determining characteristics and contractile properties of m. fibers. All m. fibers in a motor unit have identical histochemical, metabolic and physiological properties. |
| What is the speed of contraction in type I, IIa and IIb fibers? | I: slow IIa: fast IIb: fast |
| What is the size of the motor neuron in type I, IIa and IIb fibers? | I: small IIa: large IIb: large |
| What is the discharge in type I, IIa and IIb fibers? | I: low IIa: high IIb: high |
| What is the size (x-sec) difference in type I, IIa and IIb fibers? | I: small IIa: largest IIb: large |
| What is the oxidative capacity (aerobic) in type I, IIa and IIb fibers? | I: High IIa: Medium IIb: Low |
| What is the glycolytic capacity in type I, IIa and IIb fibers? | I: Low IIa: High IIb: High |
| What is the SR pumping capacity in type I, IIa and IIb fibers? | I: Low IIa: High IIb: High |
| What is the endurance level of type I, IIa and IIb fibers? | I: High IIa: Moderate IIb: Low |
| What is the capillary density in type I, IIa and IIb fibers? | I: High IIa: High IIb: Low |
| What is the myoglobin content in type I, IIa and IIb fibers? | I: High IIa: Medium IIb: Low |
| What is the myofibrillar ATPase activity in type I, IIa and IIb fibers? | I: Low IIa: High IIb: High |
| What is the glycogenolytic enzyme activity in type I, IIa and IIb fibers? | I: Low IIa: High IIb: High |
| What is the mitochondrial enzyme activity in type I, IIa and IIb fibers? | I: High IIa: Medium IIb: Low |
| What characteristics show type I as low and IIa and IIb high? (5) | 1. Discharge 2. glycolytic capacity 3. SR pumping capacity 4. myofibrillar ATPase activity 5. glycogenolytic enzyme activity |
| What 3 characteristics have type I as high, IIa as med and IIb as low? | 1. Oxidative capacity 2. Myoglobin content 3. Mitochondrial enzyme activity |
| What characteristic has type I as slow and type IIa and IIb as fast? | Speed of contraction |
| What characteristic has type I as small and IIa and IIb as large? | Motor neuron |
| What characteristic has type I as small, IIa as largest and IIb as large? | Size (x-sec) |
| What characteristic has type I as high, IIa as moderate and IIb as low? | Endurance |
| What characteristic has type I and IIa as high and IIb as low? | Capillary density |
| What can modify the metabolic profile of muscle? | Training or habitual activity influences metabolic enzymes in muscle; endurance training increases [mitochondrial enzymes] and increases mitochondrial number and volume in all fiber types. |
| What is recruitment w/ muscle activation? | Mechanism by which motor units in a muscle are progressively activated in a graded contraction. |
| How is a muscle electrically at rest? | In a completely relaxed muscle, it is electrically silent. |
| What units were recruited w/ a discharge frequency of 5-10 Hz and ~25 Hz? | Low threshold units were recruited in mild sustained contractions w/ 5-10 Hz; Increasing contraction strength made the motor units increase their discharge rate to a low maximum ~25 Hz |
| How is recruitment built up to maximal effort? | Gradually; new motor units recruited but start at higher frequency and at all levels of tension up to maximal effort. |
| How was recruitment found to occur in ballistic movements? | Recruitment order of the motor units differed from sustained contractions; high threshold units were recruited first in the case of ballistic activities. |
| What determines the maximum tension a muscle produces? | Depends on the total cross-sectional area of its muscle fibers. |
| What is the difference in hyperplasia and hypertrophy w/ strength training in muscles? | Hyperplasia: an increase in the total number of muscle fibers Hypertrophy: an increase in the diameter of existing muscle fibers |
| What muscle type gets greater enlargement during weight training? | Type II has greater enlargement since recruitment prefers type IIs more often than Is although some hypertrophy is still visible in type I fibers. |
| What other factors determine strength? | differences in bony leverages, coordination, motivation, age |
| What causes atrophy and what occurs w/ it? | Inactivity; loss of myofibrils, large decrease in mitochondria in atrophying fibers and other cell. structures. |
| What type of fibers atrophy to a greater extent? | Type I fibers to greater extant than type II during short-term periods of muscle inactivity d/t preferential recruitment, much of ADLs are type I |
| What is the adaptation in muscles seen in endurance training? | Increased resistance to fatigue in the muscles involved in the activity. |
| What increases in muscle during endurance training? (4) | 1. Increase the capacity of the fiber to produce ATP through oxidative phosphorylation 2. Increase capilarization in muscle 3. Increase myoglobin content 4. Increase mitochondrial number and enzyme concentration in muscle. |
| What muscle fiber sees the more changes with endurance training and why? | Type I; increase in number and volume of mitochondria occurs in all fiber types w/ training but a higher degree in type I; capillary density increase will affect all fiber types. |
| What is assumed of fiber types w/ endurance training? | Type IIa fibers shift metabolically to behave like type I (contributes to an improvement in performance) |
| What are 3 other factors that affect endurance? | 1. Increased cardiovascular system efficacy 2. Motivation 3. Age |
| What do metabolism and genetics have to do with the result of training? | Metabolic differences in the potential to perform aerobic or anaerobic exercise is a question of habitual use or disuse; Genetic endowment specifies the neural component, and ultimately the proportion of muscle fiber types. |
| What are the non-inflammatory muscular diseases? | 1. Muscular Dystrophy 2. Rhabdomyolysis |
| What are the inflammatory muscular diseases? | 1. Dermatomyositis 2. Polymyositis 3. Inclusion Body Myositis |
| What are muscular diseases that have no category (other)? | 1. Periodic Paralysis 2. Myositis Ossificans |
| What are the hallmarks of muscle disease? | Weakness, fatigue, stiffness, coordination issues, atrophy, m. cramps, spasms, usually not painful and all skeletal m. affected. |
| How do you DDx b/w neurological or muscular pathology? | Neuro: Test entire body, PNS including neural distribution, sensory loss, finite control movements, distal muscles and usually unilateral; Muscular: proximal mm., function issues, bilateral and symmetrical |
| What are the cellular characteristics of muscular dystrophy? | Degeneration of muscle fiber Regenerative activity Progressive fibrosis Infiltration of fatty tissue No inflammation (lose mass, pseudohypertrophy-fibrofatty infiltrate-creates mass but doesn't function as m.) |
| What is the worst case of muscular dystrophy and some basic facts? | Duchenne (DMD); most severe and rapidly progressing of the MDs; genetic in origin; Males 3:100K births; 2/3 of pt.s have relatives w/ DMD |
| In a growing child what can be seen w/ DMD? | Abnormal muscle can be observed in utero; elevated serum CK from birth; Physical problems don't manifest until 3-4 yoa; pseudohypertrophy can be observed |
| What is the generic progression of DMD? | Age 10: wheelchair bound Age 15: bedridden Age 20: death d/t respiratory deficiency (b/c diaphragm and intercostal mm. effected) |
| What is rhabdomyolysis and what is found in m. fibers w/ it? | Diffuse destruction of skeletal m. fibers, non-inflammatory degenerative process; clusters of macrophages in and around m. fibers. |
| What are risk factors for rhabdomyolysis? | alcoholism, crushing injuries, heat intolerance, heat stroke, severe exertion, trauma |
| What would an acute presentation of rhabdomyolysis present w/? | Sarcoplasmic contents are poured into circulation (large proteins have to be filtered by kidneys); myoglobinuria; acute renal failure |
| How do muscles appear w/ rhabdomyolysis and what are onset of attacks associated w/? | Muscles may be swollen and tender and many demonstrate profound weakness; the flu, mild exercise, heat stroke, alcohol intoxication |
| What drugs seem to be associated w/ rhabdomyolysis and what might Tx be? | Cocaine and statins (1% of pts who take statins get rhabdomyolysis); Tx varies but prescribe diuretics, hydration to aid kidneys |
| What is a basic description of inflammatory myopathies? | Generally rare and likely all are autoimmune based; usually associated w/ CT Dzs |
| Who is affected w/ dermatomyositis? | Adults and children, females > males |
| What occurs w/ dermatomyositis? | Compliment mediated antibodies attack microvasculature of skeletal muscle, ischemia of individual fibers, infarctions and secondary inflam., skin involved d/t microangiopathy, atrophy of m. fibers and damage to BVs, 15-40% 5 year death rate. |
| When does polymyositis onset, what cells do the damage and what is seen in the muscle? | After 20 y/o; damage d/t t-cells that directly attack muscle fibers; no microangiopathy, see necrosis, phagocytosis, regeneration (attempt) and fibrosis (fibrofatty infiltrate) |
| What is muscle inflammation in polymyositis similar to and where is degeneration? | Similar seen in HIV infection; degeneration is scattered and not always in the areas of inflammation. |
| Who is affected w/ inclusion body myositis and what is damage d/t? | M:F 3:1, onset over 50 y/o; damage d/t t-cells w/ similar mechanism to polymyositis but presence of specific antigen on sarcolemma. |
| What is the inclusion in inclusion body myositis? | Granular inclusions seen in the cytoplasm or nuclei of involved muscle fibers. |
| What are general characteristics of inflammatory myopathies? | Problems w/ simple activities that use proximal muscles, difficulty swallowing, increased serum CK and increased ESR (inflam.) |
| Is exercise good w/ inflammatory myopathies? | Traditionally it was discouraged but currently exercise believed to be beneficial since it increases muscular strength, improves cardiovascular performance and does not increase CK (counterbalance to destruction) |
| Will corticosteroids help inflammatory myopathies? | Can work well except in inclusion body myositis, which has no effective therapy. |
| What is periodic paralysis? | Varying degree of paralysis, may be mild weakness, not hysterical paralysis, inherited cond'ns related to potassium metabolism. |
| What causes periodic paralysis? | Familial, autosomal cond'n, episodes of flaccid paralysis w/ loss of DTR and no response to electric stim. |
| What are the 3 types of periodic paralysis? | 1. Hyperkalemic 2. Hypokalemic 3. Normokalemic |
| What occurs w/ hyperkalemic periodic paralysis and what is the specific cause? | Attacks last less than one hour and aggravated by previous day's exercise; genetic mutation w/ DHP recepors and channels realtive to K channel; episodes start before age 16 |
| What occurs w/ hypokalemic periodic paralysis and what is the specific cause? | General weakness of voluntary muscles, begins as young adult (<16 y/o) and improves w/ age, attacks shorter in duration, more frequent and less severe; mutation for genes for muscular Na channels |
| What occurs w/ normokalemic periodic paralysis? | Attacks last for days or weeks; least known since tests normal b/w bouts; believed that muscle surface does not propagate APs but Ca in m. fibers results in contraction |
| What is myositis ossificans and where may it occur? | Metaplasia of soft tissue to bone, mostly occurs in muscle but can occur in fascia, tendons, joint capsule and fatty tissue. |
| What are the 3 stages of myositis ossificans? | 1. Pseudosarcoma - 4-6 weeks 2. Differentiation - 2-3 months 3. Maturation - long time |
| How does the pseudosarcoma stage of myositis ossificans begin? | Trauma, crushed or torn, blunt trauma is common (collisions: vehicles, sports, etc.) |
| After the trauma in the Pseudosarcoma stage of myositis ossificans what occurs? | Massive necrosis, degeneration, regeneration, cellular proliferation w/ immature structures. |
| What occurs in the pseudosarcoma stage of myositis ossificans after the initial necrosis and damage? | Extensive damage and cell death, holes in sarcolemma sheath and fluid accumulates, phagocytes invade making holes bigger and greatest damage in center of injury. |
| What happens towards the end of the pseudosarcoma stage of myositis ossificans and how can the process be aggravated? | Damaged tissue is liquefied and replaced by sheets of non-specific cells; process can be aggravated by trauma, massage, stretching, surgery, excess activity and ultrasound. |
| What happens after about 15 days of the pseudosarcoma stage of myositis ossificans? | Extensive proliferation of mesenchymal tissue, minimal osteoid formation, looks like a neoplasia histologically and easy to confuse w/ osteosarcoma. |
| When does the differentiation stage of myositis ossificans begin? | 2-3 months post injury |
| What occurs in the differentiation stage of myositis ossificans? | Mesenchymal cells differentiate into fibro-, chondro- and osteoblasts; giant cells remove debris; periphery materializes; center may remain fluid filled cyst or filled w/ undifferentiated cells; mature bone dev. around periphery. |
| What occurs in the maturation stage of myositis ossificans? | Develops periosteum that seperates it from surrounding tissues; may remain like this indefinitely or may shrink and disappear and depending on size may be removed surgically. |
| Where is myositis ossificans associated w/ neurologic Dz found? | Seen in brain, cord or peripheral nerve Dz; pathology develops distal to neurologic leasions w/ unknown relationship. No trauma. |
| What is progressive myositis ossificans? | Rare, some inherited, usually involves mm. of the back and major joints, muscles progressively ossified; Sx begin in childhood and give a severe functional disability and is generally fatal d/t loss of pulmonary function. |
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kabrown
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